Thyrotropin‐releasing hormone stimulates a calcium‐activated potassium current in a rat anterior pituitary cell line.

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Abstract
1. The ‘giga‐seal’ patch‐electrode technique (Hamill, Marty, Neher, Sakmann & Sigworth, 1981) was used for constant current and voltage‐clamp recordings in the GH3 rat anterior pituitary cell line. 2. Thyrotropin‐releasing hormone (TRH) causes a membrane hyperpolarization that is mediated by a selective increase in K+ permeability. The hyperpolarization cannot be evoked when the cell is internally perfused with a Ca2+ chelator but persists when the external solution that bathes the cell is Ca2+‐free or contains a Ca2+‐channel blocker. 3. Under voltage clamp the TRH‐induced current is approximately linear at negative potentials (‐90 to ‐30 mV) but markedly enhanced at voltages above ‐30 mV). Thus, the affected conductance has a voltage‐dependent component. 4. The TRH‐induced increase in K+ permeability is sensitive to inhibition by 30 mM‐TEA and 200 nM‐apamin, inhibitors of two distinct Ca2+‐activated K+ permeabilities in GH3 cells. 5. The time course of the TRH‐induced K+ current is similar to the time course of a TRH‐induced transient peak elevation of cytosolic Ca2+ that is due to mobilization of Ca2+ from intracellular stores. 6. The effects of TRH on the K+ current and the rise in cytosolic Ca2+ are half‐maximal at 7 nM and 1.7 nM, respectively. 7. It is concluded that the TRH‐induced hyperpolarization is mediated by two distinct Ca2+‐activated K+ conductances that are activated by release of Ca2+ from an intracellular site.

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